Research Reports - Chronic alcoholism-mediated impairment in the medulla oblongata: a mechanism of alcohol-related mortality in traumatic brain injury?

Cell Biochem Biophys. 2013 Dec;67(3):1049-57

Lai XP, Yu XJ, Qian H, Wei L, Lv JY, Xu XH

Alcohol-related traumatic brain injury (TBI) is a common condition in medical and
forensic practice, and results in high prehospital mortality. We investigated the
mechanism of chronic alcoholism-related mortality by examining the effects of
alcohol on the synapses of the medulla oblongata in a rat model of TBI. Seventy
adult male Sprague-Dawley rats were randomly assigned to either ethanol (EtOH)
group, EtOH-TBI group, or control groups (water group, water-TBI group). To
establish chronic alcoholism model, rats in the EtOH group were given EtOH twice
daily (4 g/kg for 2 weeks and 6 g/kg for another 2 weeks). The rats also received
a minor strike on the occipital tuberosity with an iron pendulum. Histopathologic
and ultrastructure changes and the numerical density of the synapses in the
medulla oblongata were examined. Expression of postsynaptic density-95 (PSD-95)
in the medulla oblongata was measured by ELISA. Compared with rats in the control
group, rats in the chronic alcoholism group showed: (1) minor axonal
degeneration; (2) a significant decrease in the numerical density of synapses (p
< 0.01); and (3) compensatory increase in PSD-95 expression (p < 0.01). Rats in
the EtOH-TBI group showed: (1) high mortality (50%, p < 0.01); (2) inhibited
respiration before death; (3) severe axonal injury; and (4) decrease in PSD-95
expression (p < 0.05). Chronic alcoholism induces significant synapse loss and
axonal impairment in the medulla oblongata and renders the brain more susceptible
to TBI. The combined effects of chronic alcoholism and TBI induce significant
synapse and axon impairment and result in high mortality.